The Effect of Nimodipine, Indeced Hypertension, and Combined Nimodipine Therapies with Induced Hypertension on Experimental Cerebral Infarction.
- Author:
Young Ho SEO
1
;
In Hong KIM
;
Jang Chull LEE
;
Eun Ik SON
;
Dong Won KIM
;
Man Bin YIM
Author Information
1. Department of Neurosurgery, School of Medicine, Keimyung University, Taegu, Korea.
- Publication Type:Original Article
- Keywords:
Nimodipine;
Induced hypertension;
Combined therapy;
Cerebral infarction;
Middle cerebral artery occlusion
- MeSH:
Adult;
Animals;
Brain;
Cerebral Infarction*;
Dopamine;
Humans;
Hypertension*;
Infarction;
Infarction, Middle Cerebral Artery;
Nimodipine*;
Rats;
Subarachnoid Hemorrhage;
Vasospasm, Intracranial
- From:Journal of Korean Neurosurgical Society
1994;23(6):607-614
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The treatment with nimodipine is recommended as an effective therapy for the delayed ischemic neurological deficits(DIND) caused by cerebral vasospasm following aneurysmal subarachnoid hemorrhage. The induced hypertension is also widely accepted as a treatment method to reverse the DIND caused by cerebral vasospasm. Therefore, the combination of these two regimens may be considered as a more effective treatment method for the DIND than nimodipine or induced hypertension alone. The authors performed this experimental study to clear up this subject. In a series of 60 adult rats, a surgical occlusion of the middle cerebral artery(MCA) was carried out by a microsurgical technique. The animals were divided into 4 groups as follows ; group I(N=15) : control group, group II(N=15) : nimodipine treated group, group III(N=15) : induced hypertension group, group II(N=15) : combined nimodipine treated with induced hypertension group. Group II animals were treated with an infusion of nimodipine intravenously(1 microgram/Kg/min), and group III animals were maintained high blood pressure(B.P) to 160 mmHg by an infusion of dopamine intravenously(2 microgram/Kg/min), and group IV animals were treated with an infusion of nimodipine and dopamine intravenously. All animals of each group were sacrificed at 6,12 and 24 hours after MCA occlusion. Then the brain slices were obtained and stained with triphenyltetrazolium chloride(TTC). The size of the infraction area was quantified by a computer image analysis system and the size of the infraction area compared among each groups. The results showed that each size of the infraction area according to sacrifice time at 6, 12 and 24 hours after MCA occlusion was significantly smaller in group II, III, IV than that of group I(p<0.05). The total size of the infraction area was significantly smaller in group II, III and IV than that of group I(group I vs. II vs. III vs. IV ; 13.23+/-2.60 vs. 9.17+/-2.23 vs. 10.24+/-2.23 vs. 8.85+/-2.23%, respectively. group I vs. II, III and IV : p<0.05). However, there was not noticed any significant difference in the size of the infarction area among group II, III and IV. This study concludes that the treatment of the combined nimodipine with induced hypertension has no more benefit for the improving infarction in the permanent focal ischemic model than nimodipine or induced hypertension treatment alone.
